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Related Concept Videos

Intestinal Obstruction II: Pathophysiology01:07

Intestinal Obstruction II: Pathophysiology

Intestinal obstruction triggers a series of physiological responses, starting with gas and fluid accumulation in the bowel segment proximal to the obstruction, leading to distension. This distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia.To overcome the blockage, the gut intensifies contractions, causing colicky abdominal pain, nausea, and vomiting, which reduces fluid and food intake and...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
Acute Pancreatitis I: Introduction01:25

Acute Pancreatitis I: Introduction

Acute pancreatitis is the sudden inflammation of the pancreas caused by the early activation of digestive enzymes, leading to the autodigestion of pancreatic tissue. This results in local inflammation and, in severe cases, systemic complications.EtiologyUnderstanding the underlying causes is crucial, as identifying the etiology guides treatment and anticipates complications. Acute pancreatitis can be triggered by various factors, typically grouped into the following clinical categories.Biliary...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
Acute Pyelonephritis II: Diagnostic Studies and Management01:28

Acute Pyelonephritis II: Diagnostic Studies and Management

Introduction:For diagnosing acute pyelonephritis, a comprehensive patient history is collected to identify symptoms such as dysuria, frequent or urgent urination, flank pain, or costovertebral angle (CVA) tenderness that may suggest a kidney infection.Physical ExaminationDuring the physical examination, CVA tenderness is assessed. This involves gentle percussion over the costovertebral angle, where tenderness often indicates a kidney infection.Diagnostic TestsUrinalysis: Used to identify white...

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Related Experiment Video

Updated: May 23, 2026

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
05:39

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

Advanced necrotizing enterocolitis part 1: mortality.

M Thyoka1, P de Coppi, S Eaton

  • 1Department of Surgery, Great Ormond Street Hospital and UCL Institute of Child Health, London, UK.

European Journal of Pediatric Surgery : Official Journal of Austrian Association of Pediatric Surgery ... [Et Al] = Zeitschrift Fur Kinderchirurgie
|March 22, 2012
PubMed
Summary
This summary is machine-generated.

Mortality for advanced necrotizing enterocolitis (NEC) remains high at 32%, even with minimal bowel involvement. Improvements in neonatal care have not reduced death rates for this severe infant condition.

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Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
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Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

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Last Updated: May 23, 2026

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
05:39

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
06:51

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Published on: July 28, 2023

Area of Science:

  • Neonatal Surgery
  • Pediatric Gastroenterology
  • Critical Care Medicine

Background:

  • Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease in infants.
  • Advanced NEC often requires surgical intervention.
  • Mortality rates for surgical NEC have remained a concern despite advances in neonatal care.

Purpose of the Study:

  • To identify factors associated with mortality in infants undergoing surgical treatment for advanced necrotizing enterocolitis (NEC).

Main Methods:

  • A retrospective review of infants with confirmed NEC (Bell stage II or III) treated between January 2002 and December 2010.
  • Comparison of data between survivors and nonsurvivors using Mann-Whitney and Fisher's exact tests.
  • Analysis of gestational age, birth weight, gender distribution, and extent of intestinal disease.

Main Results:

  • Of 205 infants with NEC, 170 (83%) underwent surgery, and 66 (32%) died.
  • Mortality was highest in infants with pan-intestinal disease (86%) but significant in those with multifocal (39%) and focal (21%) disease.
  • Multiple organ dysfunction syndrome was the most common cause of death, with care withdrawal in nearly half of nonsurvivors.

Conclusions:

  • Overall mortality for advanced NEC remains high at 32% and has not improved over a 10-year period.
  • Significant mortality is observed even in cases with minimal bowel involvement.
  • Further strategies are needed to improve outcomes for infants with necrotizing enterocolitis requiring surgery.